Subject: Simultaneous presence of retrovirus and herpes virus could be one
of the causes of MS

And where do we get retroviruses from? Whoever was holding up their hands and
saying vaccines - give yourselves a gold star! This crap is causing just
about every ill known to humankind! When are we going to learn? And herpes -
basically a monkey virus that has adapted to humans - well, where do you
think that comes from? How many monkeys does it take to make a vaccine? A
bloody lot, that's how many! And they all carry loads of foreign viruses and
bacteria!

Department of Medical Microbiology and Immunology, University of
Aarhus,DK-8000 Aarhus C, Denmark. tb@microbiology.au.dk

Retroviruses have been suggested as possible pathogenic factors in multiple
sclerosis (MS), supported by the observation that endogenous retroviruses are
activated in MS patients. Different members of the herpes family of which
several are neurotropic have also been suggested as factors in MS
pathogenesis. Further, interactions between retroviruses and herpes viruses
have been implied in the development of MS. The objective of the study was
investigation of cell-mediated immune responses of MS patients to retrovirus
and herpes virus antigens, particularly antigen combinations, with analyses
of the influence of retrovirus antigens on cellular immunological reactivity
toward other viral antigens. Cellular immunity as measured by blast
transformation assays was analyzed using freshly isolated peripheral blood
mononuclear cells from 47 MS patients and 36 healthy volunteers. Combinations
of the endogenous retrovirus HERV-H and herpes virus antigens
resulted in highly increased cellular immune responses among both the MS
patients and healthy subjects. The increase was synergistic in character in
most samples. Very pronounced effects were obtained using HHV-6A and HSV-1
antigens. Blast transformation assays combining antigens from two different
herpes viruses or combinations of measles and herpes antigens showed no
synergy. The obtained data indicate a pronounced synergistic effect on the
cellular immune response when retrovirus and herpes antigens are present
together. The cause of the synergy is unknown so far. The effect on the
immune response may influence the disease progression.

Georgia State University's Biosafety Level (BSL)-4 lab is one of five
biomedical research facilities in the United States devoted to the study of
the world's deadliest pathogens. The lab, located in downtown Atlanta,
concentrates its efforts on the study of herpes B, a virus common to some
monkeys though rare in humans. But human contagion is not unheard of,
usually among workers at primate labs who get bit or scratched by monkeys,
and is lethal if not treated early. The other labs are part of a federal
system developing ways to combat emerging infectious diseases and preparing
for a potential bioattack, each with numerous researchers trying to create
diagnostic tests, treatments, and vaccines. The government is pushing ahead
with plans to build more BSL-4 labs at the Fort Detrick Army complex in
Maryland and in Galveston, Texas; Hamilton, Mont.; and Boston, where the
plans have met with stiff opposition from community activists and a group of
150 scientists, including two Nobel Prize winners, who question the wisdom of
building such a site in an urban landscape

Herpes Research Uncovers Possible Clue
To Alzheimer's Disease

Providence, R.I. -- Researchers at
Brown University and the Marine Biological Laboratory at Woods Hole,
Mass., have found a physical connection between the herpes simplex virus
and amyloid precursor protein, a protein that breaks down to form a
major component of the amyloid plaques that are consistently present in
the brains of persons with Alzheimer's disease.

http://www.sciencedaily.com/releases/2003/11/031107055048.htm

Amyloid precursor protein or APP breaks down to
form beta-amyloid. There is strong evidence, according to the
researchers, that beta-amyloid is the underlying cause of Alzheimer's.

While the scientists caution that no conclusions
about Alzheimer's can be drawn from their findings, Dr. Elaine Bearer,
senior research scientist and associate professor in Brown's Department
of Pathology and Laboratory Medicine, believes the work does in fact
link the common herpes virus of cold sores with the neurodegenerative
disorder. Bearer isalso a summer investigator at the Marine Biological
Laboratory at Woods Hole, Mass.

Past studies have implicated the herpes virus in the
onset of Alzheimer's disease, but agreement within the scientific
community on the value of that research is far from universal. Bearer
expects that the discovery of a physical interaction between APP and the
herpes virus will trigger further investigations into the role the virus
may play in the disease, and even into possible uses of the virus in
therapy.

The scientists stress that none of what they found
should cause alarm among those who have at one time had a cold sore.
According to Bearer, nearly 85 percent of us harbor the herpes simplex
virus and most of us never develop Alzheimer's.

The researchers discovered the interaction between
the herpes simplex virus (HSV) and APP while conducting experiments in
the giant axon of squid at the Marine Biological Laboratory. Prasanna
Satpute-Krishnan and Joseph A. DeGiorgis, both doctoral candidates in
Brown's graduate program at the time of the research, were seeking to
learn how viruses are carried around the body within cells and from one
cell to another. Specifically, they were examining how the herpes
simplex virus travels back to the lip area to form a recurring blister
after remaining latent for some time in the trigeminal ganglion, a
collection of nerve cells next to the brain.

What they found was that the herpes virus was
interacting with APP, a putative motor receptor that recruits a
microtubular motor, kinesin, for transport through neurons. This was the
first time scientists had observed any physical interaction between the
herpes virus and APP.

Without the APP, the virus moves backward up an axon
(a long extension of a neuron) from the area of the lip towards the
trigeminal ganglion. But the Brown researchers discovered that once it
interacts with the APP, the virus travels in the opposite direction what
scientists describe as anterograde transport back down to the lip. The
researchers also found that once coupled with the APP, the virus moves
remarkably fast.

"It's as if the virus hijacks a car which in this
case would be the kinesin and the APP is the driver," explains Bearer.
"The virus takes the APP where it wants to be, not where the APP wants
to be."

The build-up of beta-amyloid (formed in the breakdown
of APP) is found consistently in the brains of Alzheimer's patients, and
many scientists are now convinced it is involved in the disease,
according to Satpute-Krishnan. Questions persist, however, as to what
that involvement is, and why, when APP is found in all of us, it causes
problems only in a few.

Perhaps, Bearer speculates, when the APP is co-opted
by the herpes virus, the APP breaks down at a location where it would
not normally appear and at a very different rate. "When APP piles up
around neurons, the neurons die," she explains. "But we don't yet know
if this is a secondary or a primary cause of Alzheimer's."

"At this point, of course, we don't yet know whether
herpes plays a causal role in Alzheimer's disease," DeGiorgis notes.
"But our research does provide some interesting new insight into both
diseases."

A paper outlining the findings of the Brown/MBL
researchers titled "Fast Anterograde Transport of Herpes Simplex Virus:
Role of Amyloid Precursor Protein" will appear in the December issue of
Aging Cell, published by Blackwell Publishing in England and at the
publisher's "OnlineEarly" site [http://www.blackwell-synergy.com/links/toc/ace].

Satpute-Krishnan, the first author of the paper, is a
graduate student in Brown's Molecular Biology, Cell Biology and
Biochemistry Graduate Program. Bearer, who holds both an M.D. and a
Ph.D., is an experimental pathologist. DeGiorgis, who earned his Ph.D.
in Bearer's lab last year, is now with the National Institutes of
Health.

Experiments in this study were conducted in the giant
axon of squid, a model widely used in research because with a diameter
of nearly a millimeter it is 1,000 times thicker than a human axon.
Researchers are able to inject substances into the giant axon and then
observe the behavior of those substances through high-powered
microscopes.

"It is pretty extraordinary that breakthroughs in
Alzheimer's disease and in the pathogenesis of herpes virus should be
made using the squid of the North Atlantic sea," notes Bearer.

Last summer Brown University and the Marine
Biological Laboratory formalized their alliance for teaching and
research. The affiliation between the two institutions established the
Brown-MBL Graduate Program in Biological and Environmental Sciences. In
addition, it will promote faculty exchanges and research collaborations,
such as the one conducted by Satpute-Krishnan, DeGiorgis and Bearer.

###The affiliation between MBL and Brown takes
advantage of the geographic proximity of the two institutions, uniting
their faculty expertise in biology and medicine, particularly for
molecular biology, genomics, ecosystems studies, environmental science,
global infectious diseases, neuroscience and public health. Student
recruitment for the Brown-MBL Graduate Program got under way this fall,
with the first students expected to begin their studies next year.

MBL is an internationally known, independent,
nonprofit institution dedicated to improving the human condition through
creative research and education in the biological, biomedical and
environmental sciences. Founded in 1888, the MBL is the oldest private
marine laboratory in the Western Hemisphere

Australian researchers are developing a vaccine to prevent one of the most
common forms of physical disability. Cerebral Palsy has always been
blamed on lack of oxygen at birth but researchers now believe it's
caused by the herpes virius, passed on from the mother to the foetus.
The virus attacks developing nerve cells in the baby's brain and while
most can fight it off but about 1 in 500 have gene mutations which lower
their immunity. There is currently no way to prevent disorder but
researchers at the Women's and Children's Hospital in Sydney are working
on a vaccine which could be given to teenage girls to immunise them
against herpes virus. They're also working on how to repair the faulty
genes.